162 research outputs found
Computational and Biological Analogies for Understanding Fine-Tuned Parameters in Physics
In this philosophical paper, we explore computational and biological
analogies to address the fine-tuning problem in cosmology. We first clarify
what it means for physical constants or initial conditions to be fine-tuned. We
review important distinctions such as the dimensionless and dimensional
physical constants, and the classification of constants proposed by
Levy-Leblond. Then we explore how two great analogies, computational and
biological, can give new insights into our problem. This paper includes a
preliminary study to examine the two analogies. Importantly, analogies are both
useful and fundamental cognitive tools, but can also be misused or
misinterpreted. The idea that our universe might be modelled as a computational
entity is analysed, and we discuss the distinction between physical laws and
initial conditions using algorithmic information theory. Smolin introduced the
theory of "Cosmological Natural Selection" with a biological analogy in mind.
We examine an extension of this analogy involving intelligent life. We discuss
if and how this extension could be legitimated.
Keywords: origin of the universe, fine-tuning, physical constants, initial
conditions, computational universe, biological universe, role of intelligent
life, cosmological natural selection, cosmological artificial selection,
artificial cosmogenesis.Comment: 25 pages, Foundations of Science, in pres
Falsification Of The Atmospheric CO2 Greenhouse Effects Within The Frame Of Physics
The atmospheric greenhouse effect, an idea that many authors trace back to
the traditional works of Fourier (1824), Tyndall (1861), and Arrhenius (1896),
and which is still supported in global climatology, essentially describes a
fictitious mechanism, in which a planetary atmosphere acts as a heat pump
driven by an environment that is radiatively interacting with but radiatively
equilibrated to the atmospheric system. According to the second law of
thermodynamics such a planetary machine can never exist. Nevertheless, in
almost all texts of global climatology and in a widespread secondary literature
it is taken for granted that such mechanism is real and stands on a firm
scientific foundation. In this paper the popular conjecture is analyzed and the
underlying physical principles are clarified. By showing that (a) there are no
common physical laws between the warming phenomenon in glass houses and the
fictitious atmospheric greenhouse effects, (b) there are no calculations to
determine an average surface temperature of a planet, (c) the frequently
mentioned difference of 33 degrees Celsius is a meaningless number calculated
wrongly, (d) the formulas of cavity radiation are used inappropriately, (e) the
assumption of a radiative balance is unphysical, (f) thermal conductivity and
friction must not be set to zero, the atmospheric greenhouse conjecture is
falsified.Comment: 115 pages, 32 figures, 13 tables (some typos corrected
Accelerated expansion from structure formation
We discuss the physics of backreaction-driven accelerated expansion. Using
the exact equations for the behaviour of averages in dust universes, we explain
how large-scale smoothness does not imply that the effect of inhomogeneity and
anisotropy on the expansion rate is small. We demonstrate with an analytical
toy model how gravitational collapse can lead to acceleration. We find that the
conjecture of the accelerated expansion being due to structure formation is in
agreement with the general observational picture of structures in the universe,
and more quantitative work is needed to make a detailed comparison.Comment: 44 pages, 1 figure. Expanded treatment of topics from the Gravity
Research Foundation contest essay astro-ph/0605632. v2: Added references,
clarified wordings. v3: Published version. Minor changes and corrections,
added a referenc
Biological Sex, Sex-Role Identity, and the Spectrum of Computing Orientations: A Re-Appraisal at the End of the 90s
Idiopathic pulmonary fibrosis in BRIC countries: the cases of Brazil, Russia, India, and China
The Quantum Mitochondrion and Optimal Health
A sufficiently complex set of molecules, if subject to perturbation, will self-organise and show emergent behaviour. If such a system can take on information it will become subject to natural selection. This could explain how self-replicating molecules evolved into life and how intelligence arose. A pivotal step in this evolutionary process was of course the emergence of the eukaryote and the advent of the mitochondrion, which both enhanced energy production per cell and increased the ability to process, store and utilise information. Recent research suggest that from its inception life embraced quantum effects such as “tunnelling” and “coherence” while competition and stressful conditions provided a constant driver for natural selection. We believe that the biphasic adaptive response to stress described by hormesis – a process that captures information to enable adaptability, is central to this whole process. Critically, hormesis could improve mitochondrial quantum efficiency, improving the ATP/ROS ratio, while inflammation, which is tightly associated with the aging process, might do the opposite. This all suggests that to achieve optimal health and healthy ageing, one has to sufficiently stress the system to ensure peak mitochondrial function, which itself could reflect selection of optimum efficiency at the quantum level
Short Telomeres Compromise β-Cell Signaling and Survival
The genetic factors that underlie the increasing incidence of diabetes with age are poorly understood. We examined whether telomere length, which is inherited and known to shorten with age, plays a role in the age-dependent increased incidence of diabetes. We show that in mice with short telomeres, insulin secretion is impaired and leads to glucose intolerance despite the presence of an intact β-cell mass. In ex vivo studies, short telomeres induced cell-autonomous defects in β-cells including reduced mitochondrial membrane hyperpolarization and Ca2+ influx which limited insulin release. To examine the mechanism, we looked for evidence of apoptosis but found no baseline increase in β-cells with short telomeres. However, there was evidence of all the hallmarks of senescence including slower proliferation of β-cells and accumulation of p16INK4a. Specifically, we identified gene expression changes in pathways which are essential for Ca2+-mediated exocytosis. We also show that telomere length is additive to the damaging effect of endoplasmic reticulum stress which occurs in the late stages of type 2 diabetes. This additive effect manifests as more severe hyperglycemia in Akita mice with short telomeres which had a profound loss of β-cell mass and increased β-cell apoptosis. Our data indicate that short telomeres can affect β-cell metabolism even in the presence of intact β-cell number, thus identifying a novel mechanism of telomere-mediated disease. They implicate telomere length as a determinant of β-cell function and diabetes pathogenesis
Identification of regulatory variants associated with genetic susceptibility to meningococcal disease
Non-coding genetic variants play an important role in driving susceptibility to complex diseases but their characterization remains challenging. Here, we employed a novel approach to interrogate the genetic risk of such polymorphisms in a more systematic way by targeting specific regulatory regions relevant for the phenotype studied. We applied this method to meningococcal disease susceptibility, using the DNA binding pattern of RELA - a NF-kB subunit, master regulator of the response to infection - under bacterial stimuli in nasopharyngeal epithelial cells. We designed a custom panel to cover these RELA binding sites and used it for targeted sequencing in cases and controls. Variant calling and association analysis were performed followed by validation of candidate polymorphisms by genotyping in three independent cohorts. We identified two new polymorphisms, rs4823231 and rs11913168, showing signs of association with meningococcal disease susceptibility. In addition, using our genomic data as well as publicly available resources, we found evidences for these SNPs to have potential regulatory effects on ATXN10 and LIF genes respectively. The variants and related candidate genes are relevant for infectious diseases and may have important contribution for meningococcal disease pathology. Finally, we described a novel genetic association approach that could be applied to other phenotypes
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